EFFECTS OF ISCHEMIC AND HYPOXIC HYPOXIA ON VO2 AND LACTIC-ACID OUTPUT DURING TETANIC CONTRACTIONS

We measured O2 uptake (V̇O2), CO2 output (V̇CO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxic hypoxia (hypoxia), and free-flow normoxia (control). The major goal was to assess the effects of these perturbations of L̇ during contractions. Ischemia and hypoxia were initiated just before the start of the contractions and at minute 7 of contractions in separate groups of experiments. Whenever applied, both ischemia and hypoxia reduced V̇O2 compared with the control values. When ischemia was initiated at the start of contractions, L̇ was reduced transiently compared with the controls. When ischemia began at minute 7, L̇ was increased modestly but transiently compared with the controls. When hypoxia was initiated at the start of contractions, L̇ was increased during the entire period of contractions. The L̇ pattern was the same as in the controls, rising to a maximal value at 3 min and declining steadily to a lower value at 30 min. When hypoxia began at minute 7, L̇ declined initially at a slower rate than it did in the controls and was thereby elevated above the controls from 9 to 30 min. Ischemia was associated with a more rapid reduction in mechanical performance than hypoxia. The data suggest that the mechanisms of the decreased mechanical performance and V̇O2 are different for ischemia and hypoxia.